Neurostimulation unit for immobilizing the heart during cardiosurgical operations

ABSTRACT

The invention relates to a device for temporary reduction of heart movement during an operation, more particularly a heart operation, comprising a neurostimulation unit ( 20 ) for stimulation of the nerves ( 3 ) that slow down heart frequency, said unit including at least one electrode device ( 1 ) with at least one stimulation pole ( 2 ), wherein a control unit ( 19 ) connected to the neurostimulation device ( 20 ) is provided. Said control device has a first input device ( 26 ) for inputting a degree of immobilization and is configured to influence the operating state of the neurostimulation device ( 20 ) depending on the previously set degree of immobilization.

This invention relates to a stimulation device with which it is possibleto selectively electrically stimulate the epicardial or extracardiacparasympathetic nerves of the heart innervating the sinus node or theatrioventricular node to electrically largely immobilize the heartduring cardiac surgery by slowing the heart rate.

Cardiovascular support during cardiac surgery by means of anextracorporeal circulation of a heart-lung machine offers specificdisadvantages. Critical factors include in particular the incidence ofsystemic inflammations and immune reactions, the thrombogenic effect offoreign body material, the reduced cardiac output especially due to thepotassium cardioplegia (low-output state) and the altered flow dynamicsunder the conditions of artificial circulation (Cremer et al. Ann.Thorac. Surg. 1966; 61: 1714-20; Myles et al. Med. J. Austr. 1993; 158:675-7; Roach et al. N. Engl. J. Med; 335: 1857-63; G. M. McKhan et al.Ann. Thorac. Surg. 1997; 63: 516-521; Ede et al. Ann. Thorac. Surg.1997; 63: 721-7). The reduced perfusion to all organs of the body, inparticular during surgery, which is influenced by many of these factors,may lead to permanent organ damage such as neurophysiological andneuro-psychological damage, even including a stroke or renal failure,for example (Cremer et al. Ann. Thorac. Surg. 1966; 61:1714-20; Myles etal. Med. J. Austr. 1993; 158:675-7; Roach et al. N. Engl. J. Med.335:1857-63; G. M. McKhan et al. Ann. Thorac. Surg. 1997; 63:516-521).

Therefore, methods have been developed for creating a bypass to thecoronary vessels without requiring cardiovascular support byextracorporeal circulation using the heart-lung machine during heartsurgery.

Local stabilizers of the myocardial area in the immediate vicinity of acoronary vessel make it possible to create a coronary anastomosis on abeating heart, for example (Boonstra et al. Ann. Thorac. Surg. 1997;63:567-9).

Heart surgery with circulatory support by microaxial pumps is anothergentle alternative to surgery with the assistance of a heart-lungmachine. Microaxial pumps for cardiac support have been known for a longtime. They have a flywheel which supports the blood flow and isfrequently referred to as a rotor or impella and rotates about an axissituated coaxially in the blood vessel. European Patent EP 0 157 871 B1and European Patent EP 0 397 668 B1 describe a microaxial pump in whichthe flywheel is connected to an extracorporeal drive part via a flexibleshaft running through the catheter. The drive part drives the flexibleshaft, which in turn drives the flywheel of the microaxial pump.

Recent developments in microaxial pumps, which are already in useclinically, involve combining the drive part and the pump part in oneunit and implanting them as a unit in the vascular system of the body.Instead of the mechanically susceptible drive shaft, only a power supplycable for supplying electric power to the drive part passes through thecatheter. Such a microaxial pump, also known in general as an“intravascular blood pump” is described in German Patent DE 196 13 564C1, for example.

A pump system comprising two pumps may be used to assume all or part ofthe pumping function of the heart (described in PCT/EP/98/01868). Such asystem is capable of handling a cardiac output of approximately 4.5liters of blood per minute and can reduce an increased wall excursionduring bradycardia, for example. The pump device has a first pump, whichmay be inserted with its intake side into the left ventricle, while asecond pump, which is situated with its intake side in the right atrium,lies with its pressure side in the pulmonary artery. The two pumps areoperated by a shared control unit. The two pumps are introduced into theheart without having to open the ventricle.

A so-called “paracardial blood pump” (German Patent Application 100 16422.6-35) is also able to handle an even higher cardiac output of fiveto six liters of blood per minute, and, thus, to minimize the increasedwall excursion which occurs in bradycardia due to the fact that heartfunction is completely taken over by the pump. In contrast with the“intravascular pump” described above, this is a blood pump which drawsin blood from one part of the heart and delivers it into the aorta orsome other target region, the casing of the blood pump being applied tothe outside of the heart while the pump inlet has a direct connection tothe chamber of the heart from which the blood is drawn.

If the entire cardiac output is handled during a severe episode ofbradycardia by using the intra- or paracardial pump described above, thefluid balance is established by the sensors integrated into the pumps,allowing monitoring of the blood flow delivered in a mutual dependencyof the pumps.

In contrast with surgery using the heart-lung machine, the heart stillcontinues to beat due to the persistence of its own electricactivity—despite the fact that the cardiac output is being handled bythe blood pump—but it does so without pumping any relevant blood volume.This mechanical action makes open-heart surgery difficult and increasesthe myocardial oxygen consumption.

To minimize this movement of the heart during surgery, a stimulationdevice according to the present invention is described below with whichit is possible to selectively electrically stimulate the epicardial orextracardiac parasympathetic nerves of the heart innervating the sinusnode or the atrioventricular node to largely electrically immobilize theheart during heart surgery by reducing the heart rate. In particular,the combination of such a neurostimulation unit with intracardial orparacardial blood pumps is described to ensure perfusion of organs,including the heart, during bradycardia.

On the healthy heart, the spontaneous heart rate is determined by thepulse generation rate of the pacemaker center of the heart, theso-called sinus node. The sinus node is located on the high lateralright atrium. The electric conduction of the stimulation of the atria tothe chambers of the heart is in turn accomplished via the so-calledatrioventricular (AV) node. The vegetative autonomic nervous systemconsists of a stimulating part, the sympathetic nervous system, and asedative part, the parasympathetic nervous system. Activation of theparasympathetic nervous system causes the sinus node frequency to beslowed down (negative chronotropic effect) and leads to a delay in theatrioventricular conduction via the AV node (negative dromotropiceffect). Parasympathetic nerves innervating the sinus node and the AVnode extracardially run along the superior vena cava and along thepulmonary arteries to the sinus node or AV node and then cluster nearthe target organ in circumscribed epicardial accumulations of fat andconnective tissue (so called nerve plexus or “fat pads”). The nerveplexus, which contains almost all the parasympathetic fibers thatinnervate the sinus node, is situated epicardially on the lateral rightatrium in a corner between the right atrial wall and the right pulmonaryveins crossing behind the right atrial wall (so-called ventral rightatrial plexus). The nerve plexus which contains most of theparasympathetic nerve fibers innervating the atrioventricular node issituated in a corner between the coronary sinus ostium, the inferiorvena cava and the left atrium (the so-called inferior inter-atrialplexus). FIG. 1 shows a schematic representation of theseparasympathetic nerve plexus.

The epicardial electric stimulation of the right ventral atrial plexustriggers a sinus bradycardia without having any relevant influence onthe AV node conduction. Epicardial or transvascular electric stimulationof the inferior inter-atrial plexus slows down the atrio-ventricularconduction (P. Schauerte et al. Catheter stimulation of cardiacparasympathetic nerves in humans. A novel approach to the cardiacautonomic nervous system. Circulation, 2001; 104: 2430-2435) but has noeffect on the sinus node frequency. Epicardial or transvascularstimulation of the two nerve plexus leads to shortening of the localatrial refractory time in the vicinity of the respective nerve plexusand can result in a slight reduction in the atrial contractility.However, the ventricular pumping force or refractory time is notinfluenced significantly. The transvascular nerve stimulation thresholdsare much higher than the epicardial stimulation thresholds (P. Schauerteet al. Ventricular Rate Control During Atrial Fibrillation by CardiacParasympathetic Nerve Stimulation. A Transvenous Approach. J. Am. Coll.Cardiol. 1999; 34: 2043-2050). Parasympathetic fibers innervating thesinus node and the AV node may also be stimulated electricallyextravascularly or transvascularly along/in the vena cava, which alsoleads to negative chronotropic and dromotropic effects (P. Schauerte etal. Ventricular Rate Control During Atrial Fibrillation by CardiacParasympathetic Nerve Stimulation. A Transvenous Approach. J. Am. Coll.Cardiol. 1999; 34: 2043-2050; P. Schauerte et al. Transvenousparasympathetic nerve stimulation in the inferior vena cava andatrioventricular conduction. J. Cardiovasc. Electro-physiol. 2000; 11:64-69; P. Schauerte et al. Transvenous parasympathetic cardiac nervestimulation: An approach for stable rate control. J. CardiovascElectrophysiol. 1999; 10: 1517-1524; P. Schauerte et al. Treatment oftachycardiac atrial fibrillation by catheter-supported electricstimulation of the cardiac parasympathetic nervous system. Z Kardiol.2000; 89: 766-773; P. Schauerte et al. Transvascular radiofrequencycurrent catheter ablation of parasympathetic cardiac nerves abolishesvagally mediated atrial fibrillation. Circulation, 2000; 28: 2774-2780).

In addition, this results in shortening of the atrial refractory timebut an extension of the ventricular refractory time and a slightreduction in the atrial contractility. Parasympathetic fibersinnervating the sinus node and the AV node may also be stimulated alongthe right or left pulmonary artery, which also causes negativechronotropic and dromotropic effects. The parasympathetic fibers alongthe superior vena cava and along the pulmonary arteries arepreganglionic nerve fibers while both preganglionic and postganglionicnerve fibers accumulate in the inferior inter-atrial plexus (P.Schauerte et al. Transvascular radiofrequency current catheter ablationof parasympathetic cardiac nerves abolishes vagally mediated atrialfibrillation, Circulation, 2000; 28: 2774-2780).

FIG. 1 illustrates the effect of electric stimulation of the inferiorinteratrial plexus. The frequency-retarding effect is instantaneous,i.e., it begins immediately with the onset of nerve stimulation andterminates immediately after the end of stimulation. In addition, it is“titratable,” i.e., the extent to which the heart rate is slowed downcan be adjusted through the choice of the corresponding stimulationvoltage.

FIG. 2 shows an example of parasympathetic stimulation of the ventralright atrial plexus.

The object of the present invention is to create a device which willtemporarily reduce the heart rate or stop the heart from beating bytransient intraoperative epicardial or transvascular electricparasympathetic stimulation in order to facilitate, by this temporaryelectric reduction in heart movement, the job of the surgeon/robot inguiding the surgical instruments at the heart.

This object is achieved with the invention by a device for temporarilyreducing the movement of the heart during surgery, in particular duringcardiac surgery, with a neurostimulation unit for stimulating nervesthat slow down the heart rate, comprising at least one electrode devicehaving at least one stimulation electrode. According to the presentinvention, a control unit is connected to the neurostimulation unit,said control unit having a first input device for preselecting of adegree of immobilization and being arranged for influencing theoperating mode of the neurostimulation unit as a function of thepredetermined degree of immobilization.

Any bradycardia is normally associated with an increase in strokevolume. Therefore, intraoperative bradycardia would reduce the number ofcontractions per minute, but a single contraction would lead to agreater inward-outward movement of the wall of the heart, which wouldcounteract immobilization of the heart. In other words, frequent slightwall excursions without neural stimulation would be replaced by a fewmajor wall movements during neural stimulation.

To compensate for this disadvantage of bradycardization, this invention,in an advantageous modification provides for a combination of theneurostimulator with another movement-reducing device also beingconnected to the control unit and having the form of anintravascular/intracardiac pump which takes over a portion of themechanical pumping function of the heart. The cardiac output taken overby the pump can be adapted at any time to the extent of the bradycardia,i.e., the greater the bradycardia, the greater is the cardiac outputtransported through the pump. In this way an adequate cardiac output ismaintained during bradycardia, but at the same time the increased strokevolume and consequently the increased wall excursion of bradycardia arereduced, which results in a more effective immobilization of the heartthan that obtained with an intravascular pump or a nerve stimulationalone.

The combination of a neurostimulation unit with a movement reducingdevice in the form of a stabilization device for stabilizing the cardiacwall, e.g., a local stabilization/immobilization device, is providedaccording to the present invention. The bradycardia achieved with theneurostimulation unit and the electric immobilization should cooperateadditively to the local immobilization achieved through the localstabilization systems.

Other preferred embodiments of this invention are derived from thedependent claims and/or the description of preferred embodiments givenbelow and referring to the accompanying drawings. It is shown in:

FIG. 1 an electrocardiogram at electric stimulation of the inferiorinteratrial plexus;

FIG. 2 an electrocardiogram at parasympathetic stimulation of theventral right atrial plexus;

FIG. 3 a preferred embodiment of an electrode device of an apparatusaccording to the present invention;

FIG. 4 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 5 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 6 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 7 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 8 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 9 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 10 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 11 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 12 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 13 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 14 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIGS. 15A and 15B another preferred embodiment of an electrode device ofan apparatus according to the present invention;

FIG. 16 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 17 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 18 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 19 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 20 another preferred embodiment of an electrode device of anapparatus according to the present invention;

FIG. 21 another preferred embodiment of an apparatus according to thepresent invention;

FIG. 22 another preferred embodiment of an apparatus according to thepresent invention;

FIG. 23 a block schematic of the control loop of another preferredembodiment of the apparatus according to the present invention;

FIG. 24 a block schematic of the control loop of another preferredembodiment of the apparatus according to the present invention.

FIG. 1 shows an example of the parasympathetic stimulation of theventral right atrial plexus with consecutive sinus bradycardia (P-Pinterval 440 ms). To prevent atrial myocardial stimulation, thehigh-frequency (200 Hz) nerve stimuli (*) were triggered in the atrialrefractory time. Immediately after the end of neurostimulation (thickvertical arrow) in the atrial refractory time, there is again a rise inthe sinus node frequency (P-P interval 300 ms). R denotes the R wave andP denotes the P wave.

FIG. 2 shows the effect of epicardial electric stimulation of theinferior right atrial plexus in a dog. The frequency retarding effect isinstantaneous, i.e., it starts immediately with the onset ofneurostimulation and terminates immediately after neurostimulation isstopped. Here again, R denotes the R wave and P denotes the P wave.

According to the present invention, the neurostimulation unit comprisesan electrode device in the form of a stimulation electrode 1 which isattached epicardially to the ventral right atrial plexus, the inferiorinteratrial plexus, the superior vena cava or the right or leftpulmonary artery. The introduction of such an electrode may be performedin the open thorax after performing a thoracotomy. As an alternative,however, the neurostimulation electrodes may also be placed by trocar atthe stimulation sites endoscopically/robot controlled. In a typicalembodiment, the electrode has one or two electrically conductingstimulation poles 2.1, whose effective stimulation area amounts tobetween 1 and 100 mm² (preferred embodiment, 4-9 mm²) (see FIGS. 3-7).The stimulation poles may be part of an electric conductor (stimulationwire) insulated with plastic, the insulation being stripped off of saidconductor in the area of the stimulation pole 2. The stimulation wire ispulled through the epicardial nerve plexus 3 so that the stimulationpole 2 comes to lie within the nerve plexus. To facilitate insertioninto the nerve plexus 3, one embodiment of the stimulation wire has atapered point or needle 4, making it possible to puncture through thenerve plexus 3. In a typical embodiment, this is a (half)-round needle 4which makes it possible to puncture through the epicardial nerve plexus3 at the surface. To permit bipolar stimulation of the nerve plexus, twostimulation wires are placed in the nerve plexus 3 spaced a distance ofapprox. 2-10 mm apart. Alternatively, two mutually insulated electricconductors may be combined in a shared stimulation electrode (see FIGS.6-8). Each of the two insulated conductors has a stimulation pole 2 atdifferent distances from the electrode tip 4.

To prevent dislocation of the stimulation electrode 1 out of the nerveplexus 3, in a typical embodiment there is a locking device 5 on bothsides of the stimulation electrode 1. These may be, for example, twoplastic anchors on the two sides of the stimulation electrode 1 (seeFIGS. 3, 6, 7) or a clamp which is attached to both sides afterpositioning the electrode (see FIG. 4).

To prevent, above all, myocardial stimulation of the adjacent orsuperior ventricular myocardium especially when the inferior interatrialplexus is stimulated, in a particular embodiment, a shielding device inthe form of an insulating cap 6, which is made of a material that is notelectrically conductive, may be temporarily attached to both sides ofthe stimulation electrode 1 with a locking device 5, so that thestimulation poles 2 located within the plexus 3 and the plexus 3 areinsulated from the surrounding/superior myocardium (see FIG. 9).Alternatively, the stimulation poles 2, which are mounted on astimulation electrode 1 designed to be flat, may be electricallyshielded on one side (see FIG. 8). This makes it possible to positionthe stimulation electrode 1 with the electrically conductingsurface/side facing the epicardium and provide a shield 6 with respectto the (ventricular) myocardium above it. Likewise, the stimulationelectrode 1 may also be positioned with the electrically conductingsurface/side facing away from the epicardium so that the insulatedsurface 6 is in contact with the epicardium. This results in theelectrode 1 being positioned between the epicardium and the plexus 3above it, so that simultaneous (atrial) myocardial stimulation duringneurostimulation is prevented. In another embodiment, a stimulationelectrode 1, which is designed to be flat, may also be combined with aninsulation cap 6. In this case, however, the electrically conductingsurface of the electrode 1 is placed, in the plexus 3, facing away fromthe epicardium and the insulating cap 6 is attached to the stimulationelectrode with a locking device on both sides of the stimulationelectrode (see FIG. 9). This may prevent electric stimulation of the(atrial) myocardium which is beneath the plexus 3 as well as theventricular myocardium above it.

In another embodiment, the stimulation electrode consists of a ringelectrode 1 which is composed of two half-round arms 7 (FIGS. 10-12).The proximal ends are movably secured with the distal ends being incontact end-to-end or overlapping at the ends. The distal ends of bothsemicircles can be pulled apart by a push/pull mechanism acting on thehinge 8 of the semicircles and being transmitted through a positioningelement 9 and said distal ends behave like two forceps arms 7 which cangrip the tissue of the nerve plexus 3 (see FIG. 12A). Because of theelastic restoring forces of the two semicircles or due to a renewedforce acting on the hinge 8, the arms 7 of the circle then close and arethus secured in the nerve plexus 3. The arms 7 of the forceps thereforeact like a fastening element for securing the ring electrode 1. Thepositioning element 9 is then removed from the hinge 8 (see FIG. 12B).The two semicircles 7 are made of an electrically conducting materialand are coated with a non-electrically conducting substance except forthe distal ends. The semicircles 7 are connected to a flexible electricconductor that is electrically insulated toward the outside. By placingtwo such ring electrodes 1 in a nerve plexus 3, bipolar stimulation ispossible. According to one variant of this embodiment, two oppositeelectric poles 2 are arranged on one ring electrode 1 (see FIG. 13).

An alternative embodiment of the stimulation electrode 1 consists of athin flexible silver wire coated with Teflon, for example, with theinsulation being removed from the tip of the silver wire for a length ofapproximately 5-10 mm. This wire can be inserted through a traditionalhollow needle 10 made of steel such as those used for venous vascularpuncture (e.g., 20 gauge needle) (FIG. 14). As soon as the wireprotrudes by approximately 5 mm out of the tip of the hollow needle, thetip of the wire is bent over to form a hook at its point of departurefrom the hollow needle. The hollow needle 10, which may also be designedas a round needle, is then inserted into the nerve plexus 3 (“fat pad”)so that the wire hook from which the insulation has been stripped comesto lie within the nerve plexus. Then the needle 10 is cautiouslyretracted, so that the wire hook remains in the nerve plexus. Forbipolar electric stimulation of the nerve plexus, two of theseTeflon-coated stimulation wires 1 with the stimulation poles 2 areplaced each within a nerve plexus 3. The distance between the twostimulation poles 2 should be between 1 and 10 mm.

In a modified embodiment, the stimulation electrodes are incorporatedinto a intake device in the form of a suction bell or suction tube 11 towhich is applied a permanent vacuum to reliably secure the stimulationpoles 2 epicardially on the nerve plexus 3 or extravascularly on vessels(see FIG. 15). The suction bell 11 is in the shape of a hemisphere. Thelargest diameter of the hemisphere is 5-15 mm with a typical diameterbeing 5 mm. In a preferred variant, the suction bell 11 is made ofplastic. An inlet opening provided on the suction bell 11 which isconnected to a suction tubing through which a vacuum can be applied. Thevacuum can be applied through an external suction via a tubing orthrough a local vacuum reservoir. Such a local vacuum reservoir couldbe, for example, a small rubber ball equipped with an outlet valve andconnected to the inlet opening of the suction bell 11. When manualcompression is applied to the rubber ball, air escapes through theoutlet valve when the suction bell 11 is at the same time placed on thenerve plexus 3 and/or the blood vessel. After the compression iseliminated, the elastic restoring forces of the balloon create a vacuumwhich pulls the nerve plexus 3 into the suction bell 11 and thus resultsin the suction bell 11 and the stimulation poles 2 being secured on thenerve plexus 3 or the vessel, respectively.

On the inside of the suction bell, next to the inlet opening areprovided two metal stimulation poles which are connected to thinelectric conductors secured along the suction tubing. The suction bell11 is placed on the ventral/inferior interatrial plexus/superior venacava/right or left pulmonary artery while applying a vacuum. The vacuumcauses the fatty tissue and nerve tissue to be sucked into thehemisphere so that it comes in contact with the stimulation poles 2. Toprevent dislocation of the suction electrode, e.g., in luxation of theheart out of the pericardial sac, the vacuum may be increased briefly.According to an alternative embodiment, two stimulation electrodes areprovided on the contact surface of the suction bell 11, coming incontact with the epicardial nerve plexus 3 in the area of thecircumference of the suction bell 11. In both embodiments, the contactsurface may be planar, concave or convex to ensure a tight closure ofthe suction bell 11 with the myocardium/nerve plexus 2.

An intake device in the form of a suction tube with a central vacuumlumen 12 (e.g., in the form of a hockey stick to reach the inferiorinteratrial plexus 3) and two electrodes 2 on the head side may be usedfor epicardial neurostimulation and are also within the scope of thisinvention (see FIG. 16).

According to an alternative variant, epicardial stimulation poles aresecured by using a fibrin adhesive injection gun (see FIG. 17). The gluegun consists of two half tubes which together form a tightly sealedround tube in the form of a hockey stick. At the head end of the shortarm of this tube two round holding fixtures have been secured, these inturn holding two metal pins at each distal end of which (the end outsideof the tube) is mounted a disk-shaped stimulation pole 2. The electricconductors are mounted on the proximal ends of the pins and come out ofthe tube again at the head end of the long tube arm. First, theassembled tube having the stimulation poles 2 coming out at the headpart of the short tube arm is used as a manually guided stimulationelectrode 1 to identify the effective stimulation pole by probatoryelectric stimulation. After discovering an effective stimulation point,the stimulation pole 2 is attached. To do so, a plurality of openingsare provided on the head end of the short tube arm in addition to thepin holding bars, said openings each being connected to a smallreservoir at the long tube end via inlet channels in the form of tubularelements 13. Then, using a syringe connected to the outside of thereservoir, fibrin adhesive, for example, can be injected through thetubular elements 13 and the mouth openings on the head part of the shortarm of the tube, so that the stimulation poles 2 positioned on the nerveplexus 3 are completely surrounded by fibrin adhesive. After briefhardening of the fibrin adhesive, the half tubes are opened up andremoved so that the stimulation poles 2 together with the pins and theattached electric conductors are “welded” to the nerve plexus 3 by thefibrin adhesive. This embodiment is particularly suitable for attachingstimulation poles 2 to neurostimulation sites that are difficult toaccess such as the inferior interatrial plexus or the nerve plexusbetween the right pulmonary artery and the base of the aorta as well asthe superior vena cava.

According to another variant, a small platform 14 is provided, havingtwo or more holes provided in it through which the two stimulation poles2 on pins 1 can be pushed through (see FIG. 18). A screw 15 at or abovethe inlet opening allows the electrode pin 1 to be attached so thatdifferent lengths of the electrode pin 1 beneath the platform 14 can beachieved. The platform 14 itself has two or more intake devices in theform of suction cups 16 with which it is positioned on the epicardialnerve plexus 3. After applying a vacuum to the suction cups 16, theplatform is stabilized and secured above the nerve plexus 3. Thestimulation pins 1 are then pushed through the inlet openings to theextent that they come in contact with the nerve plexus 3 and then aresecured in this position by the locking screws on the platform 14.

According to another embodiment variant, a screw electrode 1 is anchoredin the epicardial nerve plexus 3. The screw electrode 1 has anelectrically active tip 2 as well as a second electric stimulation polein the form of a ring electrode 2 directly behind the tip 2. The screwtypically has 3-4 (2-20) windings. By screwing into the nerve plexus 3,the electrode ring directly behind the screw comes in contact with theepicardial nerve plexus 3, thus ensuring bipolar electric stimulation ofthe nerve plexus 3 (see FIG. 19).

As an alternative, the neurostimulation electrode may be made of aflexible electrode catheter 1, along the length of which are attachedone or more circular stimulation poles 2 (electrode length 2-5 mm,interelectrode spacing 2-10 mm). Between the stimulation poles 2 thereare inlet openings 17 which communicate with one another through aconnecting lumen 18 and to which a vacuum can be applied. The inletopenings 17 may also have so-called lips 19 to facilitate contact withepicardium. By applying a vacuum, the catheter is secured on theepicardial nerve plexus 3 (see FIG. 20).

In all these embodiments, the stimulation poles are connected to astimulation unit by electrically conducting wires. The stimulation unitconsists of a pulse generating unit and a starter unit.

The neurostimulation unit also includes a pulse generating unit 21, theoperation of which is described in greater detail below with referenceto FIG. 21. The pulse generating unit 21 is preferably a voltagegenerator capable of generating electric stimulation pulses. The pulseduration may be between 0 and 20 ms (typically 0.05 to 5 ms) and thestimulation frequency may be between 0 and 1000 Hz (typically 2-100 Hz).The pulse shape may be monophasic, biphasic or triphasic. Thestimulation voltage may be between 1 and 100 V. Generally, continuousepicardial/extravascular stimulation of the nerve plexus is provided. Inthe individual case, however, an intermittent pulsed neurostimulation inthe atrial/ventricular refractory time may be necessary to preventatrial/ventricular electric myocardial stimulation of the myocardiumbeneath the nerve plexus. Therefore, short bursts of high-frequencyelectric stimuli (frequency 1-100 Hz, typically 200 Hz) are triggered sothat the stimuli are coupled to the atrial P wave or ventricular R wave.The coupling interval is typically 20 ms, but it may assume any valuebetween 0 ms and 100 ms. Atrial or ventricular myocardial depolarizationas well as the subsequent refractory phase of the heart are detected bya first detection unit 28, which is connected to the control unit 19.This is accomplished either via the neurostimulation poles 2, which mayserve as sensing electrodes, or by means of endocardially orepicardially positioned atrial and/or ventricular sensing electrodes.Alternatively, the pulsed neurostimulation may also be performedtriggered at the P wave or the R wave in the surface ECG. Theatrial/ventricular sensing signals are also needed to adapt theintensity of the neurostimuli to the particular atrial/ventricularfrequency. The atrial/ventricular signals are therefore transmitted tothe control device 19 which actuates and/or triggers the pulsegenerating unit as a function of the state of the first detectiondevice.

The control unit 19 may also be connected to a second detection unit19.2 which is in turn connected to one or more measurement probes. Thesecond detection unit 30 is used here to detect the cardiac output. Inother variants of this invention, it may also be used to detect otherbiological or mechanical measured variables such as heart rate, bloodpressure, oxygen partial pressure, repolarization times, changes in theexcitation regeneration of the heart, body temperature and mechanicalmovements such as changes in the positions of the arm of a surgicalrobot or of the surgeon. A starting unit of the control unit 19 whichresponds to the detection variables starts operation of the pulsegenerating unit 21 as soon as the particular measured value is above orbelow certain limit values. According to a modification of the starterunit, the surgeon, by using a (foot) switch 26, controls the beginning,duration and intensity of the neurostimulation on the basis of themovement of the heart and/or the immobilization of the heart which isconsidered to be necessary. Thus, like a gas pedal in an automobile, byapplying a varying pressure with the foot which is exerted on a footswitch, the extent of the neurostimulation and bradycardization isadapted to the technical surgical needs at any time. Depending on thebasic heart pump function, despite the increase in stroke volume, beyonda certain extent bradycardization is associated with a reduction incardiac output. To prevent a critical reduction in circulation duringneurostimulation, biological parameters such as cardiac output, arterialoxygen partial pressure or arterial/central venous pressure aredisplayed to the surgeon so that he can then adapt the extent andduration of bradycardization to the hemodynamic needs of the patient. Inone variant of this invention, the neurostimulation intensity isautomatically reduced by the control unit 19 if the cardiac output fallsbelow a lower limit.

In addition to the present invention, which describes exclusiveparasympathetic neurostimulation to facilitate surgery on a beatingheart, according to one variant of the present invention, aneurostimulation unit is combined with systems for local mechanicalstabilization/immobilization of the myocardial area in the immediatevicinity of a coronary vessel. The electric immobilization of the heartachieved by neurostimulation is synergistic with local immobilizationthrough the use of stabilizers.

In another preferred embodiment, the neurostimulation unit is combinedwith a pump unit in the form of an intravascular or paracardial bloodpump or an extracorporeal blood pump as a component of a motion reducingdevice. The neurostimulation unit 20, which comprises the stimulationelectrode 1 and the pulse generating unit 21 is connected to a controlunit 19. The same applies for the motion reducing device 22 whichincludes the blood pump 22 and its pump control 24. The blood pump 22should first of all maintain the cardiac output which is reduced due tothe bradycardia, and, furthermore, relieve the stroke volume of a singleheartbeat, which is elevated due to the bradycardia and results in anincreased wall movement during a single contraction. To this end, in afirst operating mode, the control unit 19 automatically increases thecardiac output provided by the pump as soon as the heart rate is reduceddue to neurostimulation. In other words, the control unit 19 controlsthe movement reducing device 22 in this operating mode as a function ofthe type of stimulation and in particular the intensity of thestimulation. Furthermore, according to a modification of the combinedpump and neurostimulation system, in a second operating mode, separatemanual control of the neurostimulator 20 and the pump 23 is possible.Thus, the surgeon is able to select, depending on the needs of theoperation and by means of two foot pedals, for example, the extent ofthe mechanical relief to be provided by the blood pump 23 and/or of theelectric immobilization due to neurostimulation. In this case, theminimum required degree of pump activity and/or the maximum availabledegree of bradycardia are determined by the programmed lower limits ofthe cardiac output. Thus, for example, the degree of bradycardia cannotbe increased further due to neurostimulation if the cardiac output fallsbelow the minimum limit while at maximum pump activity. Such acombination of neurostimulation with a paracardial pump is also suitablein special cases for the heart supportive therapy over a period of weeksor even months during which a paracardial pump 23 is implanted torelieve the volume burden on the heart and allow it to recover. Sincelowering the heart rate contributes to a reduction in myocardial oxygenconsumption, the proposed invention can contribute toward recovery ofthe myocardial tissue by lowering the heart rate. In this case, theneurostimulation electrodes 1 are anchored (semi)permanently in thenerve plexus 3, e.g., by screw or clamping mechanisms at the tip of theelectrodes 1. The electrodes are then connected to a (chronically)implantable neurostimulator that contains a battery and appropriatesoftware components for cardiac neurostimulation. Such a device isdescribed in U.S. patent 2002/0026222 A1, for example. In advantageousvariants of this invention, a switching device 19.1 is connected to thecontrol unit 19 for switching between the first and the second operatingmode.

In a special embodiment of the combination of neurostimulation withintra-/paracardial blood pump 23, the outlet opening of the intracardiacpump 23 which is situated in the proximal pulmonary artery (arteriapulmonalis communis) is lengthened by adding a neurostimulationelectrode 1. The neurostimulation electrode is to be guided through aseparate lumen to the intracardiac pump 23 into the right (left)pulmonary artery, where it electrically transvascularly stimulatesparasympathetic nerves 3 that innervate the sinus node and AV node (seeFIG. 21). As an alternative, a stimulation electrode that is fixedlyconnected to the blood pump may also be positioned in the right (left)pulmonary artery as an extension of the blood pump.

In a special embodiment, the outlet opening of the blood pump itself hasa stimulation electrode 2. The outlet opening of the blood pump 23 isadvanced into the right (left) pulmonary artery and is reversiblysecured in the vessel by inflation of a balloon 25. The balloon 25 doesthereby not occlude the vessel but instead has outlet openings formaintaining the pulmonary artery flow. The balloon 25, at itscircumference, also has two stimulation poles 2, contacting with thepulmonary arterial wall as a result of inflation of the balloon and bywhich the nerves 3 situated on the outside of the pulmonary artery maybe electrically stimulated transvascularly. To ensure perfusion of thecontralateral pulmonary artery as well when advancing the outlet openinginto one of the two pulmonary arteries, the outlet tube of the bloodpump 23 has another lateral outlet opening in the area of the branchingpoint of the contralateral pulmonary artery (see FIG. 22).

The control loop for a combined electric and mechanical immobilizationis described below as an example (see FIGS. 21 and 23). With a firstinput device 26 in the form of a (foot) switch connected to the controlunit 19, the surgeon selects the extent of the desired electricimmobilization (=heart rate retardation). According to previouslycompiled dose-effect curves, a neurostimulation intensity is provided toachieve the heart rate as the target variable. This course of thestimulation dose and immobilization effect is stored in a suitablyrepresentative patient data record in a second input device 27 that isconnected to the control unit 19. The control unit influences theneurostimulation unit 20 in the manner described below depending on thepatient data record. In parallel with this, the heart rhythm (sinusrhythm or atrial fibrillation, for example) is verified and the properepicardial neurostimulation site is selected (sinus rhythm: ventralright atrial plexus; atrial fibrillations: inferior interatrial plexus).The (change in) heart rate achieved is measured by a heart ratedetection unit 28 that is connected to the control unit 19. If theactual heart rate differs from the target rate which is preselected viaa third input device 29 connected to the control unit 19, theneurostimulation intensity is automatically increased/reduced via afeedback loop. Such deviations in an individual patient-specificdose-effect curve are detected and transmitted as correction factors tothe regulating unit of the neurostimulation unit so that an individualdose-effect curve is created for the patient. The stroke volume or thecardiac output, respectively, is measured via a cardiac output detectionunit 30 in the form of a hemodynamic detection unit connected to thecontrol unit 19 and this information is transmitted together with theheart rate to a comparator unit 19.1 of the control unit 19. Saidcomparator unit compares the actual cardiac output (HZV) with thesetpoint HZV preselected by a fourth input unit 31 that is connected tothe control unit 19. Since cardiac output may decline as a result of theretardation in heart rate, the cardiac output delivered through aparacardial pump is increased in a controlled way by the control unit 19when the cardiac output falls below a critical level. Conversely, thepump HZV is automatically reduced by the control unit 19 when the heartrate increases. If mechanical immobilization is additionally desired bythe surgeon at a given extent of electric immobilization (bradycardia),then the HZV provided by the paracardial pump 23 may also be increaseddirectly by the surgeon through appropriate action on the control unit19 in order to relieve the volume burden on the heart. The definition ofthe setpoint HZV limits also includes patient-specific parameters (e.g.,co-morbidity such as cerebral vascular constriction, renal function,basal cardiac pump capacity, etc.). Such a system allows the surgeon thenecessary free choice of the degree and duration of the electricimmobilization without compromising the patient due to a consecutivelyreduced cardiac output.

In other words, the control unit 19 influences both the operating stateof the neurostimulation unit 20 as well as of the movement reducingdevice 22 in accordance with the specifications of the first throughfourth input devices 26, 27, 29 and 31 as well as the operating statesof the heart rate detection device 28 and the cardiac output detectiondevice 30.

In one exemplary embodiment with exclusive electric immobilization ofthe heart by cardiac neurostimulation, when the cardiac output dropsbelow certain critical lower limits, the reduction in heart rate due toneurostimulation is ramped down (see FIG. 24).

1. A device for temporarily reducing the movement of the heart duringsurgery, comprising: a neurostimulation device for stimulating nervesthat slow down the heart rate, having at least one electrode device withat least one stimulation pole and a control unit being connected to theneurostimulation device having a first input device for preselecting adegree of electric immobilization of the heart and being arranged forpatient specifically influencing the operation mode of theneurostimulation device as a function of the preselected degree ofelectric immobilization, wherein the first input device is arranged forvariably preselecting the degree of electric immobilization duringoperation.
 2. The device according to claim 1, wherein the stimulationpole of the electrode device has an effective stimulation area of 1 to100 mm².
 3. The device according to claim 1 wherein the electrode devicecomprises at least two stimulation poles for bipolar stimulation thatare arranged spatially separate.
 4. The device according to claim 3,wherein the stimulation poles have a distance between each other that isbetween about 2 and about 10 mm.
 5. The device according to claim 1,wherein the electrode device inserts into a nerve plexus.
 6. The deviceaccording to claim 1, wherein the electrode device comprises at leastone locking device for securing the electrode device on a locationselected from the group consisting of a nerve plexus, a blood vessel,and a combination thereof.
 7. The device according to claim 6, whereinthe at least one locking device comprises at least one fastening devicewith at least two arms for securely clamping the electrode device andwherein at least one stimulation pole is arranged in an area of a freeend of a forceps arm.
 8. The device according to claim 6, wherein thelocking device comprises at least one suction device having at least onesuction opening for fastening the electrode device to human tissue byemployment of a vacuum.
 9. The device according to claim 8, wherein thestimulation pole is situated in an area of the suction opening.
 10. Thedevice according to claim 6, wherein the locking device comprises atleast one supply channel for tissue adhesive with at least one mouthopening for securing the electrode device with the adhesive in the areaof the mouth opening.
 11. The device according to claim 10, wherein thestimulation pole is situated in the area of the mouth opening.
 12. Thedevice according to claim 1, wherein the electrode device is a screwelectrode.
 13. The device according to claim 1, wherein the electrodedevice comprises a shielding device that is provided for the stimulationpole to prevent unwanted stimulation of cardiac tissue.
 14. The deviceaccording to claim 1, wherein the neurostimulation device comprises apulse generating unit that is connected to the electrode device and isalso connected to the control unit for triggering purposes.
 15. Thedevice according to claim 14, wherein the pulse generating unitgenerates pulses that have a characteristic selecting from the groupconsisting of a duration between 0 and 20 ms, a stimulation frequencybetween 0 and 1000 Hz, a stimulation voltage between 1 and 100 V, andany combinations thereof.
 16. The device according to claim 14 whereinthe pulse generating unit provides continuous stimulation.
 17. Thedevice according to claim 14 wherein the pulse generating unit providesintermittent stimulation, generating short bursts of high-frequencypulses.
 18. The device according to claim 17, further comprising a firstdetection unit that is connected to the control unit for detecting arefractory phase of the heart, wherein the control unit operates thepulse generating unit as a function of a state of the first detectionunit.
 19. The device according to claim 18, wherein the first detectionunit comprises at least one sensing electrode that is formed by theelectrode device.
 20. The device according to one of the claim 1,further comprising at least one second detection unit connected to thecontrol unit, for detecting at least one biological or human measuredvariable, wherein the control unit influences the neurostimulationdevice as a function of a state of the second detection unit.
 21. Thedevice according to claim 1, further comprising a movement reducingdevice that is connected to the control unit, wherein the control unitinfluences an operating state of the movement reducing device.
 22. Thedevice according to claim 21, wherein the control unit is in anoperating mode selected from the group consisting of a first operatingmode, a second operating mode, and a combination thereof, and wherein:the first operating mode, the control unit influences an operating stateof the movement reducing device as a function of an operating state ofthe neurostimulation device and, and in a second operating mode, thecontrol unit separately influences the operating state of the movementreducing device and the neurostimulation device.
 23. The deviceaccording to claim 22, wherein the control unit comprises a switchingdevice for switching between the first operating mode and the secondoperating mode.
 24. The device according to claim 21 wherein themovement reducing device comprises a device selected from the groupconsisting of a pump device for supporting cardiac function, astabilization device for stabilizing the cardiac wall, and a combinationthereof.
 25. The device according to claim 21, wherein the control unitcontrols the operating state of the movement reducing device as afunction of information selected from the group consisting of a type ofstimulation of the neurostimulation device, a stimulation intensity ofthe neurostimulation device, and a combination thereof.
 26. The deviceaccording to claim 21, further comprising a second input device that isconnected to the control unit for storing at least one patient-specificdata record that is representative of a course of a stimulation dose anda immobilization effect, and wherein the control unit influences theneurostimulation device as a function of the patient data record. 27.The device according to claim 21, further comprising a heart ratedetection device that is connected to the control unit for detecting aheart rate signal that is representative of the actual heart rate,wherein the control unit influences a device selected from the groupconsisting of the neurostimulation device the movement reducing deviceand a combination thereof, as a function of a state of the heart ratedetection device.
 28. The device according to claim 27, furthercomprising a third input device that is connected to the control unitfor input of a setpoint heart rate, wherein the control unit influencesa device selected from the group consisting of the neurostimulationdevice the movement reducing device and a combination thereof, as afunction of the state of the heart rate detection device and the thirdinput device.
 29. The device according to claim 21, further comprising acardiac output detection device that is connected to the control unitfor detecting a cardiac output signal that is representative of theactual cardiac output, wherein the control unit influences a deviceselected from the group consisting of the neurostimulation device, themovement reducing device, and a combination thereof, as a function ofthe state of the cardiac output detection device.
 30. The deviceaccording to claim 29, further comprising a fourth input device that isconnected to the control unit for input of a setpoint cardiac output,wherein the control device influences a device selected from the groupconsisting of the neurostimulation device the movement reducing device,and a combination thereof, as a function of the state of the cardiacoutput detection device and the fourth input device.
 31. The deviceaccording to claim 21, wherein the movement reducing device comprises apump unit for supporting heart function, and wherein the electrodedevice of the neurostimulation device is situated on the pump unit. 32.The device according to claim 31, wherein the stimulation pole issituated on the pump unit.
 33. The device according to claim 1, whereinthe stimulation pole of the electrode device has an effectivestimulation area of 4 to 9 mm².
 34. The device according to claim 14,wherein the pulse generating unit generates pulses that have acharacteristic selected from the group consisting of a duration between0.05 to 5 ms, a stimulation frequency between 2 to 100 Hz, a stimulationvoltage between 1 and 100 V, and any combinations thereof.
 35. A methodfor temporarily reducing the movement of a patient's heart duringsurgery, comprising: pre-selecting a degree of electric immobilizationof the heart; and providing stimulation to nerves that slow down a heartrate, wherein said stimulation is patient specifically influenced as afunction of the pre-selected degree of electric immobilization, and thepre-selected degree of electric immobilization is variable duringoperation.
 36. The method according to claim 35, wherein the stimulationto the nerves is bipolar stimulation.
 37. The method according to claim35, wherein the stimulation to the nerves is provided to a nerve plexusof the nerves.
 38. The method according to claim 37, further comprisinginserting an electrode device into the nerve plexus.
 39. The methodaccording to claim 35, further comprising securing an electrode deviceon a location selected from the group consisting of a nerve plexus, ablood vessel, and a combination thereof, wherein the stimulation to thenerves is provided by the electrode device.
 40. The method according toclaim 39, wherein the electrode device is secured on the location by atechnique selected from the group consisting of applying a clampingforce, applying a suction force, applying a tissue adhesive, applying ascrew connection, and any combinations thereof.
 41. The method accordingto claim 35, further comprising shielding tissue surrounding a locationof the stimulation to the nerves to prevent unwanted stimulation ofcardiac tissue.
 42. The method according to claim 35, wherein thestimulation to the nerves is provided by stimulation pulses, wherein thestimulation pulses have a characteristic selected from the groupconsisting of a duration between 0 and 20 ms, a stimulation frequencybetween 0 and 1000 Hz, a stimulation voltage between 1 and 100 V, andany combinations thereof.
 43. The method according to claim 35, whereinthe stimulation to the nerves is provided by continuous stimulation. 44.The method according to claim 35, wherein the stimulation to the nervesis provided by intermittent stimulation, wherein the intermittentstimulation includes generating short bursts of high-frequency pulses.45. The method according to claim 35, further comprising detecting arefractory phase of the heart, wherein the stimulation to the nerves isprovided as a function of the detected refractory phase of the heart.46. The method according to claim 35, further comprising detecting atleast one biological or human measured variable, wherein the stimulationto the nerves is provided as a function of the detected biological orhuman measured variable.
 47. The method according to claim 35, furthercomprising: providing a movement reducing device; and providing anoperating mode selected from the group consisting of a first operatingmode, a second operating mode, and a combination thereof, wherein in thefirst operating mode, an operating state of the movement reducing deviceis influenced as a function of the stimulation to the nerves, and in thesecond operating mode, an operating state of the movement reducingdevice is influenced separately from the stimulation to the nerves. 48.The method according to claim 47, further comprising switching betweenthe first operating mode and the second operating mode.
 49. The methodaccording to claim 35, further comprising providing a movement reducingdevice, wherein the movement reducing device is selected from the groupconsisting of a pump device for supporting cardiac function, astabilization device for stabilizing the cardiac wall, and a combinationthereof.
 50. The method according to claim 49, further comprisingcontrolling an operating state of the movement reducing device as afunction of information selected from the group consisting of a type ofthe stimulation to the nerves, a stimulation intensity of thestimulation to the nerves, and a combination thereof.
 51. The methodaccording to claim 35, wherein the stimulation to the nerves is providedas a function of at least one patient-specific patient data record,wherein the patient-specific patient data record is representative of apatient-specific course of a stimulation dose and an immobilizationeffect.
 52. The method according to claim 35, further comprising:detecting a heart rate signal representative of the patient's actualheart rate; and controlling an application as a function of saiddetected heart rate signal, wherein the application is selected from thegroup consisting of the stimulation to the nerves, operation of amovement reducing device, and a combination thereof.
 53. The methodaccording to claim 53, further comprising: selecting a setpoint heartrate; and controlling the application as a function of said selectedsetpoint heart rate.
 54. The device according to claim 21, furthercomprising a device for detecting a cardiac output signal representativeof the patient's actual cardiac output; wherein an application iscontrolled as a function of said detected cardiac output signal, andwherein the application is selected from the group consisting ofstimulation to the nerves that slow down the heart rate, operation ofthe movement reducing device, and a combination thereof.
 55. The methodaccording to claim 35, further comprising: selecting a setpoint cardiacoutput; and controlling an application as a function of said selectedsetpoint cardiac output, wherein the application is selected from thegroup consisting of the stimulation to the nerves, operation of amovement reducing device, and a combination thereof.